Objective To explore the protective effect of isoviolanthin on hepatic fibrosis induced by carbon tetrachloride(CC14)in mice.Methods C57BL6J mice were randomly divided into blank control group,model group,isoviolanthin group and silymarin group with 6 mice in each group.The mice in last tree groups were injected with CC14 3 times every week for 12 weeks to establish the liver fibrosis model;and the isoviolanthin and silymarin groups were treated with isoviolanthin 10 mmol/(L·d)m or silymarin 100 mg/(kg·d)by gavage from 6th to 12th weeks,respectively.The serum ALT and AST levels,the body weight and liver weight were measured;HE,Masson and Sirius Red staining were preformed to evaluate the liver injury;the expression of TGF-β1 in liver tissue was detected by immunofluorescence;serum TGF-β1,IL-1β,IL-6 and TNF-α levels were detected by ELISA;the AKT/Smad2 pathway was measured by Western blotting.Results Compared with control group,the ALT and AST were increased in model group,which were markedly decreased by isoviolanthin and silymarin treatment(P<0.05).The liver weight and body weight were increased in model group,which were markedly decreased by isoviolanthin and silymarin treatment(P<0.05).HE,Masson and Sirius Red staining of liver tissue demonstrated that isoviolanthin and silymarin intervention improved the CCl4 induced liver injury.The expression of TGF-β1 in model group was higher than that in control group,while isoviolanthin and silymarin treatment decreased the TGF-β1 level.The levels of serum TGF-β1,IL-1β,IL-6 and TNF-α in the model group were significantly higher than those in control group(P<0.05),while those in isoviolanthin and silymarin groups had a significant decrease(P<0.05).There was a significant increasing in AKT/Smad2 expression in model,which was inhibited by isoviolanthin treatment.Conclusion Isoviolanthin has a protective effect on hepatic fibrosis in mice treated by CC14,which may be associated with the suppression of AKT/Smad2 pathway.
关键词
异佛莱心苷/肝纤维化/Smad2/丝氨酸/苏氨酸蛋白激酶B
Key words
isoviolanthin/hepatic fibrosis/Smad2/protein kinase B